E
Ethan J. Weiss
Researcher at University of California, San Francisco
Publications - 40
Citations - 3469
Ethan J. Weiss is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Insulin resistance & Thrombin. The author has an hindex of 17, co-authored 36 publications receiving 3067 citations. Previous affiliations of Ethan J. Weiss include University of California, Los Angeles & Johns Hopkins University School of Medicine.
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Journal ArticleDOI
A Polymorphism of a Platelet Glycoprotein Receptor as an Inherited Risk Factor for Coronary Thrombosis
Ethan J. Weiss,Paul F. Bray,Matthew Tayback,Steven P. Schulman,Thomas S. Kickler,Lewis C. Becker,James L. Weiss,Gary Gerstenblith,Pascal J. Goldschmidt-Clermont +8 more
TL;DR: A strong association was observed between the PlA2 polymorphism of the glycoprotein IIIa gene and acute coronary thrombosis, and this association was strongest in patients who had had coronary events before the age of 60 years.
Journal ArticleDOI
PAR3 is a cofactor for PAR4 activation by thrombin
Mayumi Nakanishi-Matsui,Yaowu Zheng,David J. Sulciner,Ethan J. Weiss,Matthew J. Ludeman,Shaun R. Coughlin +5 more
TL;DR: This article showed that mPAR3 does not itself mediate transmembrane signalling but instead functions as a cofactor for the cleavage and activation of mPAR4 by thrombin.
Journal ArticleDOI
Role of thrombin signalling in platelets in haemostasis and thrombosis
TL;DR: It is shown that platelets from PAR4-deficient mice failed to change shape, mobilize calcium, secrete ATP or aggregate in response to thrombin, and supports the model that mouse PAR3 (mPAR3) does not by itself mediate transmembrane signalling but instead acts as a cofactor forThrombin cleavage and activation of mPAR4.
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Hepatocyte-Specific Disruption of CD36 Attenuates Fatty Liver and Improves Insulin Sensitivity in HFD-Fed Mice
Camella G. Wilson,Jennifer L. Tran,Derek M. Erion,Nicholas B. Vera,Maria Febbraio,Ethan J. Weiss +5 more
TL;DR: In HFD-fed animals, disruption of hepatic Cd36 protects against associated systemic inflammation and insulin resistance, and CD36 directly contributes to development of fatty liver under conditions of elevated free FAs by modulating the rate of FA uptake by hepatocytes.
Journal ArticleDOI
Protease-activated Receptors 1 and 4 Are Shut Off with Distinct Kinetics after Activation by Thrombin
TL;DR: Differences in the rates at which PAR1 and PAR4 are shut off allow thrombin to trigger intracellular signaling with distinct temporal characteristics.